The goal of this research is to understand the genetical basis of spatial patterning in the cellular slime mold P. pallidum. During morphogenesis in P. pallidum, spherical masses of cells called whorls pinch off from the base of the slug at regular intervals as the fruiting body culminates. Soon after, branches form at equidistant position around the whorl equator. We seek to understand how the positions of these branches are determined. Progress towards this goal has been aided by a panel of monoclonal antibodies specific for the early events that determine branch positions. It appears that the earliest event is the uniform amplification of pattern-associated antigens over the entire surface of the incipient whorl. With time, amplification becomes restricted to the whorl equator. Eventually, the equatorial antigen segregates into a series of evenly spaced patches that become centers for branch organization. The transition from a global distribution of antigen in two dimensions to a radial, one-dimensional distribution corresponds in kinetic detail to the expectation of a model first advanced by A. Turing in 1952. We now propose to establish a genetic system in P. pallidum that will allow us to isolate patterning mutants, establish how many genes are involved, and link the altered mutant patterns to changes at the molecular and cellular level. The question of how a multicellular organism takes on its characteristic shape and form is of central importance in the biological sciences. It underlies many of the themes that run through modern medical practice. P. pallidum, because of its relative developmental simplicity and small genome size is an ideal organism for such a study. In addition to these advantages, it has a simple, well defined life cycle, there is no cell division during morphogenesis, and it has two highly regulated spatial patterns.